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  • alpha-naphthyl butyrate esterase
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  • acetylcholine
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  • acetylcholine receptor antibody
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ACE acetonitrile; acetylcholine esterase; acute cerebral encephalopathy; acute coronary event; adrenocor...
ESA Electrolysis Society of America; endocardial surface area; epidermal surface antigen; esterase; este...
NTE neuropathy target esterase; neurotoxic esterase; not to exceed
AChRs Acetylcholine Receptors
AC abdominal circumference; abdominal compression; absorption coefficient; abuse case; acetate; acetylc...
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AChE-I acetylcholine esterase inhibitors
ACh 14C)acetylcholine
[(3)H]-ACh 3)H]-acetylcholine
AcCh Acetylcholine
AcCho Acetylcholine
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  • C1-esterase inhibitor
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  • cholesterol esterase : Áö¹æ ºÐÇØ È¿¼ÒÀÇ ÀÏÁ¾. ÄÝ·¹½ºÅ×·ÑÀ» ºÐÇØÇÑ´Ù.

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acetylcholine <chemical, neurology, physiology> A chemical found in vertebrate neurons that carries information across the synaptic cleft, the space between two nerve cells.
(06 May 1997)
acetylcholine chloride A miotic, administered as an ophthalmic solution for parasympathomimetic effect; used in cataract surgery.
(05 Mar 2000)
acetylcholine receptor antibodies <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream.
Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission.
Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy.
AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis.
AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis.
Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis.
Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued.
Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears.
(29 Dec 1997)
muscarinic acetylcholine receptor Distinct from the nicotinic ACh receptor in having no intrinsic ion channel, the receptor is formed from one protein chain with 7 transmembrane regions. The receptors produce their effect via activation of GTP-binding proteins.
(18 Nov 1997)
nicotinic acetylcholine receptor Integral membrane protein of the postsynaptic membrane to which acetylcholine binds. The receptor contains an integral ion channel, as a result of binding of acetylcholine, ion channels in the subsynaptic membrane are opened. at the neuromuscular junction, the nicotinic acetylcholine receptor initiates muscle contraction. Currently the best characterised ion channel protein: made of a hetero pentamer of related subunits, although a homo pentamer is functional in insects. Structural studies show that the acetylcholine binding site and the ionic channel are part of the same macromolecular unit. The nAChR mediates rapid transduction events (1ms) whereas receptors activating G-protein coupled channels operate on slower time scales (millisecond to second range).
(18 Nov 1997)
acetanilide esterase <enzyme> Forms aniline
Registry number: EC 3.5.1.-
(26 Jun 1999)
acetylglucomannan esterase <enzyme> Catalyses release of acetic acid from o-acetylgalactoglucomannan
Registry number: EC 3.1.1.-
(26 Jun 1999)
alpha-amino acid esterase <enzyme> Converts alpha-amino acid esters and water to alpha-amino acids and alcohol
Registry number: EC 3.1.1.43
Synonym: alpha-amino acid ester hydrolase
(26 Jun 1999)
arginine esterase <enzyme> Probably refers to an aspect of a proteinase; also index to specific proteinase class
Registry number: EC 3.1.-
Synonym: me-1,arginine ester hydrolase, me-2, me 1,me 2, arginine esterase a, esterase e-ii, esterase a
(26 Jun 1999)
bis(2-ethylhexyl)phthalate esterase <enzyme> Catalyses cleavage of the mass produced plasticiser, dehp
Registry number: EC 3.1.1.-
Synonym: dehp esterase
(26 Jun 1999)
brefeldin A esterase <enzyme> Hydrolyzes brefeldin a to brefeldin a acid and also hydrolyzes ethyl valerate; 372 amino acids; amino acid sequence given in first source
Registry number: EC 3.1.1.-
(26 Jun 1999)
butyrylcholine esterase <enzyme> An enzyme that breaks down acetylcholine tostop its action.
(22 May 1997)
C1 esterase The activated first component of complement (C1).
(05 Mar 2000)
C1 esterase inhibitor An a2-neuraminoglycoprotein that inhibits the enzymatic activity of C1 esterase, the activated first component of complement. A deficiency of this inhibitor results in a lack of inhibition of C1r and C1s leading to uncontrolled activation of the complement cascade and oedema.
(05 Mar 2000)
RAG-1 esterase <enzyme> From the oil-degrading acinetobacter lwoffii rag-1; has been sequenced; when cloned in E coli confers the ability to grow on triacetin
Registry number: EC 3.1.-
(26 Jun 1999)
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